Apple showing symptoms of infection with Venturia inaequalis (scab or black spot)
Image Credit: Cecilia Deng

Venturia inaequalis infection of apple leaf (2 days post inoculation) showing germinated conidium and development of early stage, subcuticular stroma.
Image Credit: Cecilia Deng

Venturia inaequalis Cooke (Wint.) is a hemi-biotrophic fungus belonging to the Dothideomycetes. It is the causal agent of apple scab disease (known in Australasia as black spot).  V. inaequalis has a wide geographic range and is found in almost all areas where apples are grown commercially.  However, the disease is more severe in temperate countries with cool, moist climates during early spring (Bowen et al., 2011).  
The lifecycle of V. inaequalis comprises both asexual and sexual stages. V. inaequalis overwinters predominantly as pseudothecia that develop in apple leaf litter following a phase of saprobic growth after leaf abscission.  Infection is initiated in spring by ascospores that are released by rainfall from pseudothecia, this release timed to coincide with budburst.  Germinated ascospores penetrate through the cuticle and develop into multi-layered stromata that are presumed to obtain nutrients from the sub-cuticular space.  The stromata, and the conidia that they produce, cause the characteristic leaf and fruit lesions that give the disease the name of scab.  Conidia are disseminated by wind and rain from lesions and allow secondary infection to occur within the orchard throughout the fruit development period.
The severe impact that V. inaequalis has on apple production results from the very low incidence of scab that can render fruit unmarketable.  Most commercial apple cultivars are susceptible to scab.  Consequently, very intensive and therefore costly disease control is required to reduce infection in the orchard.  Fungicide spray programmes during spring and summer are required in most apple-growing regions for conventional, integrated and organic production systems.
Research into V. inaequalis and its apple host focuses on cognate effector and resistance genes. Thus far, 17 pairings have been identified (http://www.vinquest.ch/), although only two resistance genes and no effector genes have been cloned (Bus et al., 2011; Malnoy et al., 2008; Schouten et al., 2014). It is possible to transform V. inaequalis to enable functional analyses and to cross isolates differing in mating type in vitro. Thus, the pathogenicity of V. inaequalis can be dissected. In addition to the race-cultivar specificity, the host-specificity of various Venturia species is also under investigation.  Genomic comparisons between the European and Asian pear scab pathogens, V. pirina and V. nashicola are also underway, with the aim of identifying host range determinants in the related pome fruit pathogens. This work will underpin breeding strategies to support the production of durable disease resistance in pome fruit.

References:

• Bus VGM, et al. 2011. Revision of nomenclature of the differential host-pathogen interactions of Venturia inaequalis and Malus. In: Van Alfen NK, et al. eds. Annual Review of Phytopathology, Vol 49. Palo Alto, Annual Reviews. pp 391-413.
• Bowen JK, et al. 2011. Venturia inaequalis: the causal agent of apple scab. Molecular Plant Pathology 12: 105-122.
• Malnoy M, et al. 2008. Two receptor-like genes, Vfa1 and Vfa2, confer resistance to the fungal pathogen Venturia inaequalis inciting apple scab disease. Molecular Plant-Microbe Interactions 21: 448-458.
• Schouten HJ, et al. 2014. Cloning and functional characterization of the Rvi15 (Vr2) gene for apple scab resistance. Tree Genetics and Genomes 10: 251-260.